Given the absence of information about endogenous DNA damage checkpoint activation in medulloblastomas, we first employed immunohistochemical examination of the extent of phosphorylated histone H2AX, the so‐called γH2AX marker (Bonner et al., 2008; Bartkova et al., 2005a,b) widely used to globally assess the activity of the apical DNA damage‐response kinases, including ATM and ATR that phosphorylate serine residue 139 of histone H2AX in the vicinity of DNA lesions. The gene discussed is ATM; the disease is medulloblastoma.